Therapeutic opportunities for pain medicines via targeting of specific translation signaling mechanisms

Neurobiology of Pain
Salim Megat, Theodore J Price

Abstract

As the population of the world ages and as more and more people survive diseases that used to be primary causes of mortality, the incidence of severe chronic pain in most of the world has risen dramatically. This type of pain is very difficult to treat and the opioid overdose epidemic that has become a leading cause of death in the United States and other parts of the world highlights the urgent need to develop new pain therapeutics. A common underlying cause of severe chronic pain is a phenotypic change in pain-sensing neurons in the peripheral nervous system called nociceptors. These neurons play a vital role in detecting potentially injurious stimuli, but when these neurons start to detect very low levels of inflammatory meditators or become spontaneously active, they send spurious pain signals to the brain that are significant drivers of chronic pain. An important question is what drives this phenotypic shift in nociceptors from quiescence under most conditions to sensitization to a broad variety of stimuli and spontaneous activity. The goal of this review is to discuss the critical role that specific translation regulation signaling pathways play in controlling gene expression changes that drive nociceptor sensitization an...Continue Reading

Citations

Feb 26, 2019·Anesthesia and Analgesia·Vaskar DasAsokumar Buvanendran
Mar 15, 2019·Nature Reviews. Drug Discovery·Gregory R Steinberg, David Carling
Jun 24, 2019·Regional Anesthesia and Pain Medicine·Vaskar DasAsokumar Buvanendran
Nov 13, 2020·Frontiers in Pharmacology·Guadalupe Del Carmen Baeza-FloresVinicio Granados-Soto
Jan 30, 2021·Trends in Cognitive Sciences·Caroline E PhelpsFrank Porreca
Nov 19, 2020·Pharmacological Reviews·Muhammad Saad YousufTheodore J Price
Apr 24, 2021·European Journal of Medicinal Chemistry·Xin JinTao Jiang

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Methods Mentioned

BETA
footprinting
transgenic
GTPases
Nucleotide Exchange

Software Mentioned

eFFECTOR

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